1. Field of the Invention
This invention relates to surgery, and more particularly to a method for determining the synchronicity of ventricular heart wall movement throughout the cardiac cycle including ventricular contractions, systole and diastole and optimizing the synchronicity of ventricular heart wall movement including ventricular contractions during CRT therapy and during follow-up.
2. Background and Description of Prior Art
The human heart is a pump with four chambers that beat in an organized sequence. Anatomically the heart is divided into left and right sides, and upper and lower chambers. The two upper chambers are the atria and the two lower chambers are the ventricles.
In a cardiac cycle blood enters the heart from the body's venous system though the vena cava venae cavae filling the right atrium. When the heart beats, the right atrium contracts forcing blood therein through the tricuspid valve into the right ventricle. Thereafter, contraction of the right ventricle forces the blood therein through the pulmonary artery to the lungs. Oxygenated blood returns to the heart, from the lungs, through the pulmonary vein veins and enters the left atrium. Contraction of the left atrium, which normally occurs synchronously with contraction of the right atrium, forces the blood therein through the mitral valve into the left ventricle. Contraction of the left ventricle, which normally occurs synchronously with contraction of the right ventricle, forces the blood therein outward through the aorta into the vascular system.
Systole is that portion of the cardiac cycle when the ventricular muscle cells contract causing the ventricles to force blood out of the ventricles to the lungs and body. Diastole occurs sequentially to systole and is that portion of the cardiac cycle when the ventricular muscle cells relax and the ventricles re-fill with blood from the atria.
Chamber synchrony is maintained by a complex conduction system which propagates electrical impulses to the heart muscle cells. The electrical impulses initiate the atrial and ventricular contractions.
The Sino-Atrial Node (SA node) is the pacemaker for the heart and is located in an upper portion of the right atrium. Electrical impulses spread from the SA node and cause adjacent atrial cells to depolarize in a spreading wave-front, causing the right and left atria to contract and pump blood into the respective ventricles. Depolarization and contraction of the left and right atria correlates with a “P wave” on an electrocardiogram (ECG). The electrical impulse continues propagating downwardly to the Atrio-Ventricular node (AV node) which is a small mass of highly specialized cardiac muscle fibers located in a lower portion of the right atrium. The AV node is the electrical connection from the right atrium to the right and left ventricles.
The AV node distally becomes the HIS bundle which bifurcates into a right bundle branch (RBB) and a left bundle branch (LBB). The bundle branches distally divide further into a network of Purkinje fibers which are specialized cells that conduct electrical impulses faster than other cells. Electrical impulses passing through the AV node continue through the bundle branches, and into the Purkinje fiber network encompassing the right and left ventricles. Because of the density of the Purkinje fiber network and the speed with which Purkinje fibers conduct electrical impulses, in a normal healthy heart, all the ventricular muscle cells contract synchronously during systole and relax synchronously during diastole. Depolarization and contraction of the ventricles correlates with the “QRS” complex on an ECG. The synchronized contraction of the atria and ventricles enhances the heart's pumping power. Thus, the heart includes both a complex electrical network of specialized conduction tissues and a complex mechanical network of chambers and valves.
A variety of disorders prevent the heart from operating normally, and these disorders may be systolic or diastolic and may cause dyssynchrony as well as abnormal contractility and/or abnormal relaxation. Dyssynchrony is a timing abnormality. Some of these disorders are caused by degeneration of the left ventricular conduction system which may block conduction of the electrical impulses and/or may delay propagation of the electrical impulses to the heart muscle cells. For example, left or right bundle branch block (LBBB/RBBB) is a heart failure condition that occurs when the conduction of the electrical impulses to the left or right ventricle is blocked or slowed. Bundle branch block can cause dysschronous dyssynchronous ventricular contractions which may result in heart failure. Intra-ventricular conduction delay (IVCD) is a heart failure condition that occurs when the propagation of the electrical impulses to the ventricles is “slowed down” by regional injury to myocardial tissue or by damaged Purkinje fibers that conduct the impulses slower than healthy Purkinje fibers.
When the left ventricular conduction system is damaged or “disconnected” the left ventricle muscle cells may still be excited eccentrically through muscle tissue conduction of the electrical impulses. Unfortunately, muscle tissue conduction is slower than Purkinje fiber network conduction and is also sequential. As a result, contraction of the affected portions of the left ventricle occurs in stages, rather than synchronously. For example, if a lateral wall of the left ventricle is affected by the conduction disorder, the muscle cells of the lateral wall will contract later than the muscle cells of the septal wall which is activated through normal Purkinje fiber conduction. Such dyssynchronous contraction degrades the contractility (pumping power) of the left ventricle and decreases the efficiency of the heart, which can result in, or exacerbate, heart failure.
Because the left ventricle pumps oxygenated blood to the body, a person's health is dependent upon the efficiency of the left ventricle. There are two primary methods of assessing the efficiency and pumping ability of the left ventricle; measuring Ejection Fraction, and measuring Shortening Fraction. Damage to the heart's electrical conduction system or damage to the heart's chambers and valves causes a decrease in Ejection Fraction and a decrease in Shortening Fraction.
Ejection Fraction measures the difference in the volume of blood within the left ventricle at the diastolic state, and at the systolic state, and compares the two volumes as a percentage. A normal Ejection Fraction range is 63-77% for males and 55-75% for females. Ejection Fraction percentage is determined with the following formula:
            (                                                                  Left                ⁢                                                                  ⁢                Ventricle                ⁢                                                                  ⁢                Diastolic                ⁢                                                                  ⁢                Volume                            -                                                                          Left              ⁢                                                          ⁢              Ventricle              ⁢                                                          ⁢              Systolic              ⁢                                                          ⁢              Volume                                          )        ×    100        Left    ⁢                  ⁢    Ventricle    ⁢                  ⁢    Diastolic    ⁢                  ⁢    Volume  
Shortening Fraction percentage measures the change in the diameter of the left ventricle between the systolic state and the diastolic state and is determined with the following formula:
            (                                                                  Left                ⁢                                                                  ⁢                Ventricle                ⁢                                                                  ⁢                End                            -                              Diastolic                ⁢                                                                  ⁢                Diameter                            -                                                                                          Left                ⁢                                                                  ⁢                Ventricle                ⁢                                                                  ⁢                End                            -                              Systolic                ⁢                                                                  ⁢                Diameter                                                        )        ×    100              Left      ⁢                          ⁢      Ventricle      ⁢                          ⁢      End        -          Diastolic      ⁢                          ⁢      Diameter      
A Shortening Fraction greater than 30% is considered normal. A decrease in shortening fraction usually precedes a decrease in ejection fraction. Timing of systole and diastole also provides measures of cardiac performance.
Cardiac Resynchronization Therapy (CRT), also called biventricular pacing, has been shown to improve the symptoms of ventricular dysschrony dyssynchrony and abnormal contractility and improve heart failure symptoms. CRT uses biventricular pacing to synchronize left ventricular contraction by sending electrical impulses to the heart through surgically implanted electrical leads. The timing intervals of these electrical impulses is known as Pacing Intervals. It is well recognized in the field that multiple programmable parameters, and differing pacing configurations may also be employed/applied to optimize therapy.CRT is currently indicated for patients with left ventricular systolic dysfunction, an ejection fraction of less than 35%, a prolonged QRS complex of >120 msec and severe heart failure (New York Heart Association classification III and IV) despite maximal medical therapy.
Unfortunately, only about 65% to 70% of patients who meet the above criteria respond positively to CRT and the lack of positive response may be due to sub-optimal lead placement and/or suboptimal pacing configuration. Sub-optimal lead placement and/or suboptimal pacing configuration may occur because there is presently no dynamic testing of the lead positions and/or suboptimal pacing configuration to determine physiologic response to CRT. Further, testing of the lead positions is not performed to provide baseline measures of ventricular heart wall movement, ventricular dysschrony dyssynchrony, contractility or fractional shortening. As a result it is difficult to assess whether there is baseline dyssynchrony and whether there is improvement in ventricular heart wall movement, ventricular synchronicity, contractility and fractional shortening with current CRT implant techniques using empirically positioned leads and/or empirically programmed pacing configurations.
What is needed is a method to optimize the benefits of CRT therapy, to ensure optimal lead placement by dynamic assessment of lead locations during intrinsic or baseline rhythm and during biventricular paced rhythm and to provide objective measures to determine procedure effectiveness.
Our method for optimizing CRT therapy resolves various of the aforementioned drawbacks. Our method provides a tool for practitioners to objectively determine whether biventricular pacing provides physiologic benefits to the patient by allowing dynamic assessment of the motion of the ventricular leads, and therefore the motion of the ventricle walls, and provides measures of dyssynchrony, contractility and fractional shortening and ventricular heart wall movement throughout the cardiac cycle. The provided measures allow assessment during intrinsic heart rhythm, to establish baseline focal dyssynchrony, ventricular heart wall motion and fractional shortening throughout the cardiac cycle, as well as biventricular paced heart rhythm to determine focal physiologic response to CRT therapy (i.e. changes in focal dyssynchrony, ventricular heart wall motion and fractional shortening). Our method can be utilized prognostically as a test for focal dysschrony dyssynchrony and response to pacing at temporary lead locations and with differing pacing configurations, and for optimizing CRT therapy at implant. Our method allows optimization of lead position and/or pacing configuration to improve patient outcomes based on physiologic assessment during the CRT procedure and during follow-up. Our method also allows assessment of systole and diastole which may guide therapy for heart failure.
Our invention does not reside in any one of the identified features individually but rather in the synergistic combination of all of its features, which give rise to the functions necessarily flowing therefrom as hereinafter specified and claimed.